Steady-state cerebral glucose concentrations and transport in the human brain

Understanding the mechanism of brain glucose transport across the blood-brain barrier is of importance to understanding brain energy metabolism. The specific kinetics of glucose transport have been generally described using standard Michaelis-Menten kinetics. These models predict that the steady-state glucose concentration approaches an upper limit in the human brain when the plasma glucose level is well above the Michaelis-Menten constant for half-maximal transport, Kt. In experiments where steady-state plasma glucose content was varied from 4 to 30 mM, the brain glucose level was a linear function of plasma glucose concentration. At plasma concentrations nearing 30 mM, the brain glucose level approached 9 mM, which was significantly higher than predicted from the previously reported Kt of approximately 4 mM (p < 0.05). The high brain glucose concentration measured in the human brain suggests that ablumenal brain glucose may compete with lumenal glucose for transport. We developed a model based on a reversible Michaelis-Menten kinetic formulation of unidirectional transport rates. Fitting this model to brain glucose level as a function of plasma glucose level gave a substantially lower Kt of 0.6 +/- 2.0 mM, which was consistent with the previously reported millimolar Km of GLUT-1 in erythrocyte model systems. Previously reported and reanalyzed quantification provided consistent kinetic parameters. We conclude that cerebral glucose transport is most consistently described when using reversible Michaelis-Menten kinetics.     

Lactate turnover in rat glioma measured by in vivo nuclear magnetic resonance spectroscopy

Elevated tissue lactate concentrations typically found in tumors can be measured by in vivo nuclear magnetic resonance (NMR) spectroscopy. In this study, lactate turnover in rat C6 glioma was determined from in vivo 1H NMR measurements of [3-13C]lactate buildup during steady-state hyperglycemia with [1-13C]glucose. With this tumor model, a narrow range of values was observed for the first-order rate constant that describes lactate efflux, k2 = 0.043 +/- 0.007 (n = 12) SD min-1. For individual animals, the standard error in k2 was small (< 18%), which indicated that the NMR data fit the kinetic model well. Lactate measurements before and after infusing [1-13C]glucose showed that the majority of the tumor lactate pool was metabolically active. Signals from 13C-labeled glutamate in tumors were at least 10-fold smaller than the [3-13C]lactate signal, whereas spectra of the contralateral hemispheres revealed the expected labeling of [4-13C]glutamate, as well as [2-13C] and [3-13C]glutamate, which indicates that label cycled through the tricarboxylic acid cycle in the brain tissue. Lack of significant 13C labeling of glutamate was consistent with low respiratory metabolism in this glioma. It is concluded that lactate in rat C6 glioma is actively turning over and that the kinetics of lactate efflux can be quantified noninvasively by 1H NMR detection of 13C label. This noninvasive NMR approach may offer a valuable tool to help evaluate tumor growth and metabolic responsiveness to therapies.     

Increased hepatic fatty acid polyunsaturation precedes ectopic lipid deposition in the liver in adaptation to high-fat diets in mice

Objective

We monitored hepatic lipid content (HLC) and fatty acid (FA) composition in the context of enhanced lipid handling induced by a metabolic high-fat diet (HFD) challenge and fasting.

Materials and methods

Mice received a control diet (10% of kilocalories from fat, N = 14) or an HFD (45% or 60% of kilocalories from fat, N = 10 and N = 16, respectively) for 26 weeks. A subset of five mice receiving an HFD (60% of kilocalories from fat) were switched to the control diet for the final 7 weeks. At nine time points, magnetic resonance spectroscopy was performed in vivo at 14.1 T, interleaved with glucose tolerance tests.

Results

Glucose intolerance promptly developed with the HFD, followed by a progressive increase of fasting insulin level, simultaneously with that of HLC. These metabolic defects were normalized by dietary reversal. HFD feeding immediately increased polyunsaturation of hepatic FA, before lipid accumulation. Fasting-induced changes in hepatic lipids (increased HLC and FA polyunsaturation, decreased FA monounsaturation) in control-diet-fed mice were not completely reproduced in HFD-fed mice, not even after dietary reversal.

Conclusion

A similar adaptation of hepatic lipids to both fasting and an HFD suggests common mechanisms of lipid trafficking from adipose tissue to the liver. Altered hepatic lipid handling with fasting indicates imperfect metabolic recovery from HFD exposure.

     

高亮度LED应用为驱动电路带来新的机遇和挑战

目前,业界对高亮度(HB)LED的市场预测存在很大差别。尽管预测数据不同,但趋势是明显的:高亮度LED市场正在以惊人的速度增长。有些预测数据为年复合增长率15%,另一些则为35%。2007年汽车领域的LED照明处于起步阶段,销售额为6.7亿美元,但是预计将以15%的年复合增长率增长,到2011年达到12亿美元。如果将非汽     

Eddy current effects on a clinical 7T-68 cm bore scanner

Introduction  

Eddy currents induced by switching of magnetic field gradients can lead to distortions in short echo-time spectroscopy or diffusion weighted imaging. In small bore magnets, such as human head-only systems, minimization of eddy current effects is more demanding because of the proximity of the gradient coil to conducting structures.     

透过最新世代驱动器达到高亮度LED应用

如何将新一代LED之优点发挥得淋漓尽致,则是照明系统设计人员最大的挑战之一.由于LED通常要求精准及高效率的直流电源及调光方式,因此LED 驱动 IC之设计必须能符合广泛的多变需求.电源解决方案必须效果显著、功能健全、精巧简洁,并符合经济效益.     

汽车显示器需要更明亮的背光照明

随着汽车工业和半导体工业的不断发展,人们对车内电子系统有了更高的要求.车内各种仪表、显示器的效果和品质越来越被人们所看重.高亮度LED因其良好的性能和发光效率,成为车内各种仪表、显示器背光照明的最佳选择.     

ESMRMB 2009 Congress,Antalya, Turkey, 1–3 October: Abstracts,Thursday

Object  To determine whether glycine can be measured at 7 T in human brain with ¹H magnetic resonance spectroscopy (MRS). Materials and methods  The glycine singlet is overlapped by the larger signal of myo-inositol. Density matrix simulations were performed to determine the TE at which the myo-inositol signal was reduced the most, following a single spin-echo excitation. ¹H MRS was performed on an actively shielded 7 T scanner, in five healthy volunteers. Results  At the TE of 30 ms, the myo-inositol signal intensity was substantially reduced. Quantification using LCModel yielded a glycine-to-creatine ratio of 0.14 ± 0.01, with a Cramér–Rao lower bound (CRLB) of 7 ± 1%. Furthermore, quantification of metabolites other than glycine was possible as well, with a CRLB mostly below 10%. Conclusion  It is possible to detect glycine at 7 T in human brain, at the short TE of 30 ms with a single spin-echo excitation scheme.